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Antioxidants
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Oxidative Stress in Eye Diseases
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Oxidative Stress in Eye Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 November 2025) | Viewed by 17317

Special Issue Editors

Prof. Dr. Dhirendra Pratap Singh

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Guest Editor
Ophthalmology and Visual Sciences, University of Nebraska Medical Center, Omaha, NE 68198, USA
Interests: aging and oxidative stress; antioxidants; reactive oxygen species and molecular signaling; small molecules and therapeutic targets; redox mechanisms and gene regulation
Special Issues, Collections and Topics in MDPI journals
Dr. Eri Kubo

E-Mail Website
Guest Editor
Department of Ophthalmology, Kanazawa Medical University, Kahoku District, Ishikawa, Japan
Interests: cataract; posterior capsular opacification; oxidative stress; epithelial-to mesenchymal transition; antioxidant; antiglycation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent pioneering research in redox biology has enhanced our comprehension of the role of reactive oxygen species (ROS)-induced oxidative stress in aging, as the deterioration of the cellular antioxidant defense system is a significant contributor to the development of visual impairments such as glaucoma, age-related macular degeneration, and cataracts. Nevertheless, despite a wealth of information demonstrating the role of oxidative stress in the induction of aging-related blinding diseases, the molecular mechanisms involved in the onset of oxidative-induced pathology are poorly understood. Also, the causes for excessive intracellular ROS production and dysregulation of the antioxidant defense system, leading to different types of cell death, like apoptosis, pyroptosis, ferroptosis, and so on, and their connection to ocular pathologies, remain elusive. Thus, there is a need to delineate the molecular mechanisms involved between oxidative stress and cell death types and identify the responsible culprit factors(s) to develop target-based therapeutics.

This Special Issue of Antioxidants will focus on studies on unveiling the molecular mechanism of oxidative stress/aging-induced pathological signaling and identify the involved culprit factors causing onset of ocular pathology for a structured tailored approach to manage or treat oxidative-/age-related blinding disorders.

Prof. Dr. Dhirendra Pratap Singh
Dr. Eri Kubo
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • oxidative stress
  • antioxidants
  • reactive oxygen species
  • redox signaling, inflammatory cell death
  • age-related blinding diseases
  • glaucoma
  • cataract
  • age-related macular degeneration
  • gene regulation
  • retinal disorder
  • dry eye disorder
  • corneal diseases

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Related Special Issue

Published Papers (7 papers)

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Research

Jump to: Review

27 pages, 2342 KB  
Article
TXNIP-Deficiency and Prdx6 Delivery Inhibit Aging/Oxidative Stress–Driven TXNIP-Nlrp3 Inflammasome Activation and Mitigate Pyroptosis in Lens Epithelial Cells
by Bhavana Chhunchha, Eri Kubo, Renuka R. Manoharan, Rakesh Kumar and Dhirendra P. Singh
Antioxidants 2026, 15(2), 170; https://doi.org/10.3390/antiox15020170 - 28 Jan 2026
Cited by 1 | Viewed by 1118
Abstract
Deregulated Nlrp3 (NOD-like receptor pyrin 3) inflammasome activation is strongly associated with age-related blinding diseases, including cataract. Previously, we demonstrated that loss of peroxiredoxin6 (Prdx6) promotes reactive oxygen species (ROS) amplification and aberrant activation of Klf9 and Nlrp3 inflammasome activity–driven pyroptosis. In this [...] Read more.
Deregulated Nlrp3 (NOD-like receptor pyrin 3) inflammasome activation is strongly associated with age-related blinding diseases, including cataract. Previously, we demonstrated that loss of peroxiredoxin6 (Prdx6) promotes reactive oxygen species (ROS) amplification and aberrant activation of Klf9 and Nlrp3 inflammasome activity–driven pyroptosis. In this study, using aging mouse(m)/human(h) lenses and lens epithelial cells (LECs), we reveal a critical link between Nlrp3 and thioredoxin (TRX)-interacting protein (TXNIP), which increases during aging and oxidative stress conditions. We found that aging lenses exhibiting opacity showed elevated ROS levels, increased TXNIP expression, along with upregulation of Nlrp3 inflammasome components, including caspase-1, ASC, IL-1β, IL-18, and gasderminD (GSDMD), with significantly reduced TRX1. mLECs overexpressing TXNIP were more susceptible to hydrogen peroxide (H2O2), Lipopolysaccharide (LPS), ultraviolet B (UVB)-induced oxidative stress, displaying increased ROS accumulation, reduced cell viability, and enhanced activation of Nlrp3 inflammasome and its downstream inflammatory mediators, hallmarks of pyroptotic cell death. Conversely, TXNIP knockdown suppressed Nlrp3 inflammasome activation, decreased ROS production, and significantly improved cell survival, indicating a protective effect against oxidative injury. Ex vivo, TAT-HA-Prdx6 delivery inhibited H2O2-induced Nlrp3 activation and preserved lens transparency, demonstrating its potent antioxidant and anti-inflammatory effects. Collectively, these findings identify TXNIP as a key regulator of Nlrp3 inflammasome signaling and thereby highlight the therapeutic potential of TXNIP silencing (ShTXNIP) or TAT-HA-Prdx6 delivery to halt Nlrp3-mediated pyroptosis during aging or oxidative stress conditions. Full article
(This article belongs to the Special Issue Oxidative Stress in Eye Diseases)
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16 pages, 286 KB  
Article
Oxidative Stress and Inflammatory Biomarkers in Aqueous Humor and Blood of Patients with Leber’s Hereditary Optic Neuropathy
by Berta Sánchez-Fernández, Pablo Zamorano-González, Elisa Martín-Montañez, Carmen Alba-Linero, Francisca Rius-Díaz, María García-Fernandez, Rafael Luque-Aranda and Ignacio García-Basterra
Antioxidants 2026, 15(1), 51; https://doi.org/10.3390/antiox15010051 - 30 Dec 2025
Viewed by 762
Abstract
Leber’s hereditary optic neuropathy (LHON) is a mitochondrial disorder that causes visual impairment due to the degeneration of retinal ganglion cells. Oxidative stress (OS) and inflammatory cytokines have been implicated in its pathophysiology. We investigated, for the first time, the presence of OS [...] Read more.
Leber’s hereditary optic neuropathy (LHON) is a mitochondrial disorder that causes visual impairment due to the degeneration of retinal ganglion cells. Oxidative stress (OS) and inflammatory cytokines have been implicated in its pathophysiology. We investigated, for the first time, the presence of OS biomarkers and inflammatory cytokines in the aqueous humor and peripheral blood of LHON patients compared to controls, aiming to identify potential clinical biomarkers for diagnosis and disease monitoring. A total of 38 participants were enrolled in a single-center, retrospective observational study, including 17 genetically confirmed LHON patients from different Spanish regions and 21 controls. OS biomarkers and inflammatory cytokines were quantified using spectrophotometry and fluorimetry techniques. Statistical analyses were performed to compare groups and to assess the discriminatory performance of biomarkers in identifying affected individuals. Compared to controls, LHON patients exhibited significantly higher levels of AOPP, LOOH, nitrotyrosine, GPX, GRD, and OX/AntiOX ratio in both aqueous humor and serum. Among these, serum LOOH levels and the OX/AntiOX ratio were the most reliable for identifying patients affected, with high sensitivity and specificity. However, additional data on serum IL-1ra are required to confirm its potential as an effective classifier. These findings highlight novel candidate biomarkers for the diagnosis and monitoring of LHON progression. Full article
(This article belongs to the Special Issue Oxidative Stress in Eye Diseases)
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18 pages, 8370 KB  
Article
High-Fructose High-Fat Diet Renders the Retina More Susceptible to Blue Light Photodamage in Mice
by Meng-Wei Kao, Wan-Ju Yeh, Hsin-Yi Yang and Chi-Hao Wu
Antioxidants 2025, 14(8), 898; https://doi.org/10.3390/antiox14080898 - 22 Jul 2025
Cited by 2 | Viewed by 1979
Abstract
Retinal degeneration is associated with dietary factors and environmental light exposure. This study investigated the effects of a high-fructose high-fat (HFHF) diet on susceptibility to blue light (BL)-induced retinal damage. Male ICR mice were randomized into three groups: control, BL alone, and BL [...] Read more.
Retinal degeneration is associated with dietary factors and environmental light exposure. This study investigated the effects of a high-fructose high-fat (HFHF) diet on susceptibility to blue light (BL)-induced retinal damage. Male ICR mice were randomized into three groups: control, BL alone, and BL plus HFHF diet (BL + HFHF). The BL + HFHF group consumed the HFHF diet for 40 weeks, followed by 8 weeks of low-intensity BL exposure (465 nm, 37.7 lux, 0.8 μW/cm2) for 6 h daily. The BL group underwent the same BL exposure while kept on a standard diet. Histopathological analysis showed that, under BL exposure, the HFHF diet significantly reduced the number of photoreceptor nuclei and the thickness of the outer nuclear layer and inner/outer segments compared to the BL group (p < 0.05). While BL exposure alone caused oxidative DNA damage, rhodopsin loss, and Müller cell activation, the combination with an HFHF diet significantly amplified the oxidative DNA damage and Müller cell activation. Moreover, the HFHF diet increased blood–retinal barrier permeability and triggered apoptosis under BL exposure. Mechanistically, the BL + HFHF group exhibited increased retinal advanced glycated end product (AGE) deposition, accompanied by the activation of the receptor for AGE (RAGE), NFκB, and the NLRP3 inflammasome-dependent IL-1β pathway. In conclusion, this study underscores that unhealthy dietary factors, particularly those high in fructose and fat, may intensify the hazard of BL and adversely impact visual health. Full article
(This article belongs to the Special Issue Oxidative Stress in Eye Diseases)
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27 pages, 3515 KB  
Article
Antioxidant Activity and Cytotoxicity Evaluation of New Catechol Hydrazinyl-Thiazole Derivatives as Potential Protectors in Retinal Degenerative Processes
by Răzvan-Geo Antemie, Gabriel Marc, Raluca Pele, Ionel Fizeșan, Ionuț-Valentin Creștin, Raluca Borlan, Panagiotis Theodosis-Nobelos, Eleni A. Rekka, Ovidiu Oniga, Ovidiu Crișan, Adrian Pîrnău, Laurian Vlase and Simona Valeria Clichici
Antioxidants 2025, 14(6), 646; https://doi.org/10.3390/antiox14060646 - 28 May 2025
Cited by 2 | Viewed by 4703
Abstract
Retinal degenerative processes such as age-related macular degeneration are at the center of many ongoing research studies, as their impact on the general population is significant, with severe visual impairment and even irreversible vision loss if left untreated. Currently, there are few efficient [...] Read more.
Retinal degenerative processes such as age-related macular degeneration are at the center of many ongoing research studies, as their impact on the general population is significant, with severe visual impairment and even irreversible vision loss if left untreated. Currently, there are few efficient treatments available to stop or limit its progression. In the present paper, a molecular hybridization approach was employed to develop novel compounds that address this issue. By adding either 2-butenal or a β-ionone-derived residue to the hydrazone-catechol-thiazole scaffold, two compounds were designed and synthesized: 5a and 5b. After being characterized by mass spectrometry and nuclear magnetic resonance, and proving potent antioxidant activity in the in vitro assays, the cytotoxicity evaluation using the ARPE-19, BJ, and A549 cell lines revealed a surprisingly low-dose effect of 5a and the unexpected cytotoxic activity of 5b, despite its β-ionone moiety, known for its significant therapeutic properties. Full article
(This article belongs to the Special Issue Oxidative Stress in Eye Diseases)
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19 pages, 6004 KB  
Article
Resveratrol Protects Photoreceptors in Mouse Models of Retinal Degeneration
by Shujuan Li, Hongwei Ma and Xi-Qin Ding
Antioxidants 2025, 14(2), 154; https://doi.org/10.3390/antiox14020154 - 28 Jan 2025
Cited by 2 | Viewed by 2831
Abstract
Photoreceptor/retinal degeneration is the major cause of blindness. Induced and inherited mouse models of retinal degeneration are valuable tools for investigating disease mechanisms and developing therapeutic interventions. This study investigated the potential of the antioxidant resveratrol to relieve photoreceptor degeneration using mouse models. [...] Read more.
Photoreceptor/retinal degeneration is the major cause of blindness. Induced and inherited mouse models of retinal degeneration are valuable tools for investigating disease mechanisms and developing therapeutic interventions. This study investigated the potential of the antioxidant resveratrol to relieve photoreceptor degeneration using mouse models. Clinical studies have shown a potential association between thyroid hormone (TH) signaling and age-related retinal degeneration. Excessive TH signaling induces oxidative stress/damage and photoreceptor death in mice. C57BL/6 (rod-dominant) and Nrl−/− (cone-dominant) mice at postnatal day 30 (P30) received triiodothyronine (T3) via drinking water (20 µg/mL) with or without concomitant treatment with resveratrol via drinking water (120 µg/mL) for 30 days, followed by evaluation of photoreceptor degeneration, oxidative damage, and retinal stress responses. In experiments using Leber congenital amaurosis model mice, mother Rpe65−/− and Rpe65−/−/Nrl−/− mice received resveratrol via drinking water (120 µg/mL) for 20 days and 10–13 days, respectively, beginning on the day when the pups were at P5, and pups were then evaluated for cone degeneration. Treatment with resveratrol significantly diminished the photoreceptor degeneration induced by T3 and preserved photoreceptors in Rpe65-deficient mice, manifested as preserved retinal morphology/outer nuclear layer thickness, increased cone density, reduced photoreceptor oxidative stress/damage and apoptosis, reduced upregulation of genes involved in cell death/inflammatory responses, and reduced macroglial cell activation. These findings demonstrate the role of oxidative stress in photoreceptor degeneration, associated with TH signaling and Rpe65 deficiency, and support the therapeutic potential of resveratrol/antioxidants in the management of retinal degeneration. Full article
(This article belongs to the Special Issue Oxidative Stress in Eye Diseases)
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Review

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27 pages, 1756 KB  
Review
Polyphenol-Loaded Nanodevices as Innovative Therapeutic Strategies for Dry Eye Disease: Advances and Perspectives
by Raffaele Conte, Ilenia De Luca, Anna Calarco, Mauro Finicelli and Gianfranco Peluso
Antioxidants 2025, 14(11), 1280; https://doi.org/10.3390/antiox14111280 - 25 Oct 2025
Cited by 3 | Viewed by 2012
Abstract
Background: Dry Eye Disease (DED) is a multifactorial ocular disorder characterized by tear film instability, inflammation, oxidative stress, and ocular surface damage. Current therapeutic options often provide only temporary relief and are limited by poor patient compliance and inadequate drug retention at the [...] Read more.
Background: Dry Eye Disease (DED) is a multifactorial ocular disorder characterized by tear film instability, inflammation, oxidative stress, and ocular surface damage. Current therapeutic options often provide only temporary relief and are limited by poor patient compliance and inadequate drug retention at the ocular surface. Aim: This review aims to critically analyze the therapeutic potential of polyphenols and their nanoencapsulated formulations for the management of DED, focusing on pharmacological mechanisms, formulation strategies, and translational implications. Methods: A comprehensive literature search was conducted in PubMed, Scopus, and Web of Science databases using combinations of the following keywords: “dry eye disease,” “polyphenols,” “antioxidants,” “nanocarriers,” “ocular delivery,” and “bioavailability.” Studies published in English from 2000 to 2024 were considered. Inclusion criteria encompassed experimental, preclinical, and clinical studies evaluating polyphenol-based formulations for ocular application, while reviews without original data or studies unrelated to DED were excluded. Results: The analysis identified EGCG, curcumin, resveratrol, and quercetin as the most extensively investigated polyphenols, exhibiting antioxidant, anti-inflammatory, and cytoprotective activities through modulation of cytokines, reactive oxygen species, and immune signaling pathways. Nanoformulations such as lipid nanoparticles, micelles, and cyclodextrin complexes improved solubility, stability, ocular retention, and bioavailability, leading to enhanced therapeutic efficacy in preclinical DED models. Conclusions and Future Perspectives: Polyphenol-loaded nanocarriers represent a promising approach for improving the management of DED by enhancing local drug delivery and sustained release. However, further clinical studies are needed to assess long-term safety, scalability, and regulatory feasibility. Future research should focus on optimizing formulation reproducibility and exploring personalized nanotherapeutic strategies to overcome interindividual variability in treatment response. Full article
(This article belongs to the Special Issue Oxidative Stress in Eye Diseases)
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29 pages, 1416 KB  
Review
Restoring Glutathione Homeostasis in Glycation-Related Eye Diseases: Mechanistic Insights and Therapeutic Interventions Beyond VEGF Inhibition
by Yong Chool Boo
Antioxidants 2025, 14(6), 731; https://doi.org/10.3390/antiox14060731 - 14 Jun 2025
Cited by 4 | Viewed by 2784
Abstract
Advanced glycation end-products (AGEs) and oxidative stress are recognized as central contributors to the pathogenesis of age-related or diabetic cataracts, diabetic retinopathy (DR), and age-related macular degeneration (AMD). These glycation-related diseases are characterized by impaired redox balance and decreased glutathione (GSH) levels. This [...] Read more.
Advanced glycation end-products (AGEs) and oxidative stress are recognized as central contributors to the pathogenesis of age-related or diabetic cataracts, diabetic retinopathy (DR), and age-related macular degeneration (AMD). These glycation-related diseases are characterized by impaired redox balance and decreased glutathione (GSH) levels. This review aims to examine the mechanistic links between AGEs and GSH depletion across ocular tissues by integrating in vitro, ex vivo, in vivo, and clinical studies relevant to this topic. The multiple levels of evidence highlight GSH homeostasis as both a biomarker and therapeutic target in glycation-related ocular disorders. Therapeutic strategies aimed at restoring GSH homeostasis under glycation stress are categorized into four mechanistic domains: (I) promoting GSH supply and synthesis, (II) enhancing GSH recycling, (III) mitigating glycation stress, and (IV) reducing oxidative and nitrosative stress. Most of these strategies have been explored via different approaches, and experimental findings with various interventions have shown promise in restoring GSH balance and mitigating AGE-induced damage. A pathological link between GSH depletion and vascular endothelial growth factor (VEGF) overexpression is observed in DR and wet AMD. GSH-centered interventions act upstream to modulate redox homeostasis while anti-VEGF therapies target downstream angiogenesis. This study supports the rationale for a dual-targeting strategy that combines redox-based interventions with VEGF inhibition in glycation-related ocular diseases. Full article
(This article belongs to the Special Issue Oxidative Stress in Eye Diseases)
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